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butanedione/hypoxie
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Effect of 2,3-butanedione monoxime on myocyte resting force during prolonged metabolic inhibition.
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The chemical phosphatase 2,3-butanedione monoxime (BDM) has been reported to inhibit both Ca(2+)-induced myofilament force development and rigor due to ATP depletion. However, during prolonged hypoxia in cultured ventricular myocytes BDM delays but does not prevent a marked increase in resting
Dissociation of hypoxia-induced calcium gain and rise in resting tension in isolated rat hearts.
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When isolated hearts are perfused with substrate-free hypoxic buffer for prolonged periods of time, resting tension and tissue Ca increase. These two events may be interrelated. Isolated rat hearts were used to establish whether the hypoxia-induced increase in tissue Ca can be dissociated from the
Hypoxia-targeting copper bis(selenosemicarbazone) complexes: comparison with their sulfur analogues.
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The first copper bis(selenosemicarbazone) complexes have been synthesized, using the ligands glyoxal bis(selenosemicarbazone), pyruvaldehyde bis(selenosemicarbazone), and 2,3-butanedione bis(selenosemicarbazone). Their spectroscopic properties indicate that they are structurally analogous to their
Effects of 2,3-butanedione monoxime (BDM) on contracture and injury of isolated rat myocytes following metabolic inhibition and ischemia.
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The relationship between myocardial cell contracture and injury during total metabolic inhibition (amylobarbital and iodoacetic acid) and ischemia was examined, using 5-50 mM butanedione monoxime (BDM) as an inhibitor of contracture. BDM had no apparent effect on control myocytes during 180 min
64Cu-CTS: A Promising Radiopharmaceutical for the Identification of Low-Grade Cardiac Hypoxia by PET.
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The subtle hypoxia underlying chronic cardiovascular disease is an attractive target for PET imaging, but the lead hypoxia imaging agents (64)Cu-2,3-butanedione bis(N4-methylthiosemicarbazone) (ATSM) and (18)F-fluoromisonidazole are trapped only at extreme levels of hypoxia and hence are
Cardiac hypoxia imaging: second-generation analogues of 64Cu-ATSM.
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Myocardial hypoxia is an attractive target for diagnostic and prognostic imaging, but current approaches are insufficiently sensitive for clinical use. The PET tracer copper(II)-diacetyl-bis(N4-methylthiosemicarbazone) ((64)Cu-ATSM) has promise, but its selectivity and sensitivity could be improved
Sniffing out the hypoxia volatile metabolic signature of Aspergillus fumigatus.
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Invasive aspergillosis (IA) is a life-threatening infectious disease caused by fungi from the genus Aspergillus, with an associated mortality as high as 90% in certain populations. IA-associated pulmonary lesions are characteristically depleted in oxygen relative to normal lung tissue, and it has
ATP-sensitive K+ channel activation provides transient protection to the anoxic turtle brain.
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There is wide speculation that ATP-sensitive K+ (KATP) channels serve a protective function in the mammalian brain, being activated during periods of energy failure. The aim of the present study was to determine if KATP channels also have a protective role in the anoxia-tolerant turtle brain. After
Prevention of the oxygen paradox in hypoxic-reoxygenated hearts.
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Reoxygenation after 60 min substrate-free hypoxic perfusion (modified Tyrode solution, 37 degrees C) caused isolated Langendorff hearts (from rats) to rapidly develop hypercontracture and sarcolemmal disruptions indicated by massive and sudden loss of enzymes ("oxygen paradox"). Reoxygenation (30
Adenosine and ATP-sensitive potassium channels modulate dopamine release in the anoxic turtle (Trachemys scripta) striatum.
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Excessive dopamine (DA) is known to cause hypoxic/ischemic damage to mammalian brain. The freshwater turtle Trachemys scripta, however, maintains basal striatal DA levels in anoxia. We investigated DA balance during early anoxia when energy status in the turtle brain is compromised. The roles of
A cellular mechanism for impaired posthypoxic relaxation in isolated cardiac myocytes. Altered myofilament relaxation kinetics at reoxygenation.
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Single, isolated rat ventricular myocytes were made hypoxic for 10 minutes and then reoxygenated. During hypoxia, there was a marked abbreviation of the mechanical twitch, without a decrease in its amplitude. Immediately after reoxygenation, both the time to peak shortening and the duration of
Temporary contractile blockade prevents hypercontracture in anoxic-reoxygenated cardiomyocytes.
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Reoxygenation after 120-min substrate-free anoxia causes sudden hypercontracture in isolated rat cardiomyocytes. Reoxygenated-hypercontracted cardiomyocytes maintain their sarcolemmal integrity as indicated by the absence of enzyme release and reestablish a nearly normal free energy change of ATP
The role of calcium in the toxic effects of tert-butyl hydroperoxide on adult rat cardiac myocytes.
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Oxidant stress has been implicated in reoxygenation damage following hypoxia and can lead to loss of membrane integrity and cell death. In this study the effects of oxidant stress, induced by tert-butyl hydroperoxide (tBHP), on cell conformation and intracellular free calcium ([Ca2+]i) of cardiac
Protection of reoxygenated cardiomyocytes against osmotic fragility by nitric oxide donors.
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In ischemic-reperfused myocardium, myocardial cells are jeopardized not only by reoxygenation-induced hypercontracture but also by the development of a transsarcolemmal osmotic gradient. Here the question of whether osmotic fragility of cardiomyocytes can be reduced by interventions during
Hypoxic preconditioning of cardiomyocytes and cardioprotection: phophorylation of HIF-1alpha induced by p42/p44 mitogen-activated protein kinases is involved.
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OBJECTIVE: To elucidate the molecular mechanisms involved in hypoxic preconditioning (HPC) of neonatal rat cardiomyocytes against hypoxia/reoxygenation (H/R) injury. METHODS: Cardiomyocytes from neonatal Sprague-Dawley rats were randomly distributed into the following experimental groups: (1) HPC
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